scholarly journals Measuring the human ventilatory and cerebral blood flow response to CO2: a technical consideration for the end-tidal-to-arterial gas gradient

2016 ◽  
Vol 120 (2) ◽  
pp. 282-296 ◽  
Author(s):  
Michael M. Tymko ◽  
Ryan L. Hoiland ◽  
Tomas Kuca ◽  
Lindsey M. Boulet ◽  
Joshua C. Tremblay ◽  
...  
Keyword(s):  
Blood Flow ◽  
Minute Ventilation ◽  
Linear Regression Analysis ◽  
Blood Gases ◽  
Prediction Equation ◽  
Flow Response ◽  
Arterial Blood ◽  
Reactivity Test ◽  
End Tidal ◽  
Gas Gradients

Our aim was to quantify the end-tidal-to-arterial gas gradients for O2 (PET-PaO2) and CO2 (Pa-PETCO2) during a CO2 reactivity test to determine their influence on the cerebrovascular (CVR) and ventilatory (HCVR) response in subjects with (PFO+, n = 8) and without (PFO−, n = 7) a patent foramen ovale (PFO). We hypothesized that 1) the Pa-PETCO2 would be greater in hypoxia compared with normoxia, 2) the Pa-PETCO2 would be similar, whereas the PET-PaO2 gradient would be greater in those with a PFO, 3) the HCVR and CVR would be underestimated when plotted against PETCO2 compared with PaCO2, and 4) previously derived prediction algorithms will accurately target PaCO2. PETCO2 was controlled by dynamic end-tidal forcing in steady-state steps of −8, −4, 0, +4, and +8 mmHg from baseline in normoxia and hypoxia. Minute ventilation (V̇E), internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood velocity (MCAv), and temperature corrected end-tidal and arterial blood gases were measured throughout experimentation. HCVR and CVR were calculated using linear regression analysis by indexing V̇E and relative changes in Q̇ICA, and MCAv against PETCO2, predicted PaCO2, and measured PaCO2. The Pa-PETCO2 was similar between hypoxia and normoxia and PFO+ and PFO−. The PET-PaO2 was greater in PFO+ by 2.1 mmHg during normoxia ( P = 0.003). HCVR and CVR plotted against PETCO2 underestimated HCVR and CVR indexed against PaCO2 in normoxia and hypoxia. Our PaCO2 prediction equation modestly improved estimates of HCVR and CVR. In summary, care must be taken when indexing reactivity measures to PETCO2 compared with PaCO2.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

scholarly journals Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

2014 ◽  
Vol 35 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Christopher K Willie ◽  
Philip N Ainslie ◽  
Ivan Drvis ◽  
David B MacLeod ◽  
Anthony R Bain ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Blood Gases ◽  
Arterial Oxygen ◽  
Breath Hold ◽  
Cerebral Oxygen ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
End Tidal ◽  
The Brain

The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers ( n=17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing (‘clamp’) was then used to replicate an identical temporal pattern of decreasing arterial PO2 (PaO2) and increasing arterial PCO2 (PaCO2) while breathing. End-apnea PaO2 ranged from 23  to 37 mm Hg (30±7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54±24% versus 34±26%, respectively; however, CBF increased similarly between apnea and clamp (93.6±28% and 83.4±38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

Effect of different levels of hyperoxia on breathing in healthy subjects

1996 ◽  
Vol 81 (4) ◽  
pp. 1683-1690 ◽  
Author(s):  
Heinrich F. Becker ◽  
Olli Polo ◽  
Stephen G. McNamara ◽  
Michael Berthon-Jones ◽  
Colin E. Sullivan
Keyword(s):  
Healthy Subjects ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Normal Subjects ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
End Tidal ◽  
Dose Dependent ◽  
Different Levels

Becker, Heinrich F., Olli Polo, Stephen G. McNamara, Michael Berthon-Jones, and Colin E. Sullivan. Effect of different levels of hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683–1690, 1996.—We have recently shown that breathing 50% O2 markedly stimulates ventilation in healthy subjects if end-tidal [Formula: see text]([Formula: see text]) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O2 for 30 min, with[Formula: see text] being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O2 experiment was repeated without controlling[Formula: see text] in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (V˙i) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O2 without any control on[Formula: see text] led to a 16% increase inV˙i, but[Formula: see text] decreased by 3.6 Torr (9%). There was a linear correlation ( r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, withV˙i more than doubling after 30 min of 75% O2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial[Formula: see text]. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.

End tidal-to-arterial CO2 and O2 gas gradients at low- and high-altitude during dynamic end-tidal forcing

2015 ◽  
Vol 308 (11) ◽  
pp. R895-R906 ◽  
Author(s):  
Michael M. Tymko ◽  
Philip N. Ainslie ◽  
David B. MacLeod ◽  
Chris K. Willie ◽  
Glen E. Foster
Keyword(s):  
Partial Pressure ◽  
High Altitude ◽  
Vascular Reactivity ◽  
Blood Gases ◽  
Future Research ◽  
Similar Extent ◽  
Tidal Forcing ◽  
Arterial Blood ◽  
End Tidal ◽  
Gas Gradients

We sought to characterize and quantify the performance of a portable dynamic end-tidal forcing (DEF) system in controlling the partial pressure of arterial CO2 (PaCO2) and O2 (PaO2) at low (LA; 344 m) and high altitude (HA; 5,050 m) during an isooxic CO2 test and an isocapnic O2 test, which is commonly used to measure ventilatory and vascular reactivity in humans ( n = 9). The isooxic CO2 tests involved step changes in the partial pressure of end-tidal CO2 (PetCO2) of −10, −5, 0, +5, and +10 mmHg from baseline. The isocapnic O2 test consisted of a 10-min hypoxic step (PetO2 = 47 mmHg) from baseline at LA and a 5-min euoxic step (PetO2 = 100 mmHg) from baseline at HA. At both altitudes, PetO2 and PetCO2 were controlled within narrow limits (<1 mmHg from target) during each protocol. During the isooxic CO2 test at LA, PetCO2 consistently overestimated PaCO2 ( P < 0.01) at both baseline (2.1 ± 0.5 mmHg) and hypercapnia (+5 mmHg: 2.1 ± 0.7 mmHg; +10 mmHg: 1.9 ± 0.5 mmHg). This Pa-PetCO2 gradient was approximately twofold greater at HA ( P < 0.05). At baseline at both altitudes, PetO2 overestimated PaO2 by a similar extent (LA: 6.9 ± 2.1 mmHg; HA: 4.5 ± 0.9 mmHg; both P < 0.001). This overestimation persisted during isocapnic hypoxia at LA (6.9 ± 0.6 mmHg) and during isocapnic euoxia at HA (3.8 ± 1.2 mmHg). Step-wise multiple regression analysis, on the basis of the collected data, revealed that it may be possible to predict an individual's arterial blood gases during DEF. Future research is needed to validate these prediction algorithms and determine the implications of end-tidal-to-arterial gradients in the assessment of ventilatory and/or vascular reactivity.

scholarly journals Cerebral blood flow autoregulation in ischemic heart failure

2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Healthy Volunteers ◽  
Neurological Complications ◽  
Ischemic Heart ◽  
Step Response ◽  
Ischemic Heart Failure ◽  
Arterial Blood ◽  
End Tidal

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

Ventilatory responses of hamsters and rats to hypoxia and hypercapnia

1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel
Keyword(s):  
Duty Cycle ◽  
Minute Ventilation ◽  
Natural Habitat ◽  
Blood Gases ◽  
Atmospheric Conditions ◽  
Arterial Blood Gases ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Rat Experiments ◽  
Fossorial Species

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).

scholarly journals Effects of electrical muscle stimulation on cerebral blood flow

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Soichi Ando ◽  
Yoko Takagi ◽  
Hikaru Watanabe ◽  
Kodai Mochizuki ◽  
Mizuki Sudo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Effect Size ◽  
Minute Ventilation ◽  
Voluntary Exercise ◽  
Muscle Stimulation ◽  
Electrical Muscle Stimulation ◽  
Involuntary Muscle Contraction ◽  
End Tidal ◽  
Electrical Muscle

Abstract Background Electrical muscle stimulation (EMS) induces involuntary muscle contraction. Several studies have suggested that EMS has the potential to be an alternative method of voluntary exercise; however, its effects on cerebral blood flow (CBF) when applied to large lower limb muscles are poorly understood. Thus, the purpose of this study was to examine the effects of EMS on CBF, focusing on whether the effects differ between the internal carotid (ICA) and vertebral (VA) arteries. Methods The participants performed the experiments under EMS and control (rest) conditions in a randomized crossover design. The ICA and VA blood flow were measured before and during EMS or control. Heart rate, blood pressure, minute ventilation, oxygen uptake, and end-tidal partial pressure of carbon dioxide (PETCO2) were monitored and measured as well. Results The ICA blood flow increased during EMS [Pre: 330 ± 69 mL min−1; EMS: 371 ± 81 mL min−1, P = 0.001, effect size (Cohen’s d) = 0.55]. In contrast, the VA blood flow did not change during EMS (Pre: 125 ± 47 mL min−1; EMS: 130 ± 45 mL min−1, P = 0.26, effect size = 0.12). In the EMS condition, there was a significant positive linear correlation between ΔPETCO2 and ΔICA blood flow (R = 0.74, P = 0.02). No relationships were observed between ΔPETCO2 and ΔVA blood flow (linear: R = − 0.17, P = 0.66; quadratic: R = 0.43, P = 0.55). Conclusions The present results indicate that EMS increased ICA blood flow but not VA blood flow, suggesting that the effects of EMS on cerebral perfusion differ between anterior and posterior cerebral circulation, primarily due to the differences in cerebrovascular response to CO2.

Continuous Airway Pressure Breathing With the Head-Box in the Newborn Lamb: Effects on Regional Blood Flows

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Airway Pressure ◽  
Left Ventricular Pressure ◽  
Blood Gases ◽  
Ocular Blood Flow ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Blood Flows ◽  
Arterial Blood

Continuous airway pressure delivered by a head-box is an accepted means of treating clinical hyaline membrane disease. To investigate hemodynamic alterations resulting from its use, eight newborn lambs, 1 to 6 days of age, were studied at 6 and 11 mm Hg of positive pressure, while spontaneously breathing room air. Organ blood flows and cardiac output were measured with 25 µ-diameter radioactive microspheres. Heart rate, left ventricular pressure, and arterial blood gases did not change during the study. Jugular venous pressures increased from 6.4 mm Hg to 18.6 and 24.2 mm Hg at 6 and 11 mm Hg, respectively (P &lt; .005). Cardiac output decreased approximately 20% at either intrachamber pressure setting. Renal blood flow fell 21% at 11 mm Hg. No significant changes in blood flow were found in the brain, gastrointestinal tract, spleen, heart, or liver when compared to control flows. Of particular interest was the finding of a 28% reduction in ocular blood flow at 6 mm Hg and 52% at 11 mm Hg. From these results, we conclude that substantial cardiovascular alterations may occur during the application of head-box continuous airway pressure breathing, including a significant reduction in ocular blood flow.

Abstract 10355: Physiologic Effect of Repeated Epinephrine Doses During Cardiopulmonary Resuscitation: A Randomized Porcine Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bjarne Madsen Härdig ◽  
Michael Götberg ◽  
Malin Rundgren ◽  
Matthias Götberg ◽  
David Zughaft ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Blood Gases ◽  
Brain Perfusion ◽  
Saline Control ◽  
Control Group ◽  
Arterial Blood ◽  
Pressure Peak ◽  
Blood Pressures ◽  
Lactate Levels ◽  
End Tidal

Objectives and Method: This porcine study was designed to explore the effect of repetitive epinephrine (EPI) doses on physiologic parameters during CPR. Thirty-six adult pigs were randomized to four injections of: EPI 0.02 mg/kg/dose, EPI 0.03 mg/kg/dose or saline control, given during 15 minutes of CPR. The effect on systolic, diastolic and mean arterial blood pressures (ABP), cerebral perfusion pressure (CePP), end tidal carbon dioxide (ETCO2), SpO2, cerebral tissue oximetry (SctO2), were analyzed immediately prior to each injection and at peak arterial systolic pressure. Arterial blood gases was analyzed after the baseline and after 15 min. Result: Prior to and following 4 minutes of baseline chest compressions without drug administration, there were no significant differences between the three groups. In the group given a 0.02 mg/kg/dose, there were increases in all ABP’s and CePP at the first 3 pressure peaks; at the 4th only mean ABP was increased. Decreased ETCO2 following peak 1 and beyond was seen. SctO2 and SpO2 were lowered following injection 2 and beyond. In the group given a 0.03 mg/kg/dose, all ABP’s and CePP increased at the first 3 pressure peaks. Lower ETCO2 was seen at peak 1 and beyond. SctO2 and SpO2 were lower following injection 2 and beyond. In the saline control group the systolic ABP was significantly lower at pressure peak 1 and beyond, no other parameter changed significantly compared to baseline. In the two EPI groups, pH and Base Excess were lower and lactate levels higher compared to baseline as well as compared to control. Conclusion: Repetitive EPI doses increased ABP’s and CePP, but this did not translate into better organ or brain perfusion.

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